Tat-NR2Baa TFA
Tat-NR2BAA TFA is the control peptide of Tat-NR2B9c (HY-P0117), inactive. The sequence of Tat-NR2BAA TFA is similar to Tat-NR2B9c, but it has a double-point mutation in the COOH terminal tSXV motif, making it incapable of binding PSD-95. Tat-NR2B9c is a membrane-permeant peptide and disrupts PSD-95/NMDAR binding, correlate with uncoupling NR2B- and/or NR2A-type NMDARs from PSD-95.
For research use only. We do not sell to patients.
- Formula: C105H185F3N42O31
- Molecular Weight:2588.85
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All iGluR Isoforms
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Biological Activity
Description
IC50 & Target
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NMDA Receptor |
In Vitro
Tat-NR2BAA TFA (125 ng; 20 mins) does not effects interactions between PSD-95 and NR2B subunits. In contrast, coimmunoprecipitation of PSD-95 with NR2B subunits is markedly decreased in rats pretreated with the disrupting peptide Tat-NR2B9c in lumbar dorsal horn tissue[1].Tat-NR2BAA TFA (125 ng or 1.25 μg; 20 minutes before collection of lumbar dorsal horn tissue) is the control group of Tat-NR2B9c. Tat-NR2B9c produces a significant and robust reduction of postdischarge, indicating the hyperexcitability of the cell.But Tat-NR2BAA TFA has no effects, even at a dose 100× greater than the active peptide Tat-NR2B9c (HY-P0117)[1].Tat-NR2BAA TFA (1 μM; pre-treatment 1 hour) is the control group in the Co-IP assay. Tat-NR2B9c (1 μM) disrupts NR2B/PSD95 interaction, and the coupling of NR2B to PSD-95 is more sensitive than NR2A/PSD95 to disruption in hippocampal neurons[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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Molecular Weight 2588.85
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Formula C105H185F3N42O31
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Sequence
Tyr-Gly-Arg-Lys-Lys-Arg-Arg-Gln-Arg-Arg-Arg-Lys-Leu-Ser-Ser-Ile-Glu-Ala-Asp-Ala
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Sequence Shortening
YGRKKRRQRRRKLSSIEADA
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Genotoxicity/Mutagenicity Study
The bacterial reverse mutation assay detects point mutations that restore amino-acid prototrophy in auxotrophic Salmonella typhimurium or Escherichia coli tester strains; after exposure to a test article, mutagenic activity is read out as an increased number of revertant colonies on minimal agar compared with the vehicle control. The assay uses tester strains with different mutation targets so that base-substitution and frameshift mutagens can be detected, and testing is performed with and without exogenous mammalian metabolic activation because some chemicals require biotransformation to become mutagenic.
Purity & Documentation
References
[1]. Michelle Aarts, et al. Treatment of Ischemic Brain Damage by Perturbing NMDA Receptor- PSD-95 Protein Interactions. Science [Content Brief]
[2]. Jing Fan, et al. N-methyl-D-aspartate Receptor Subunit- And Neuronal-Type Dependence of Excitotoxic Signaling Through Post-Synaptic Density 9. J Neurochem. 2010 Nov;115(4):1045-56. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)